ocularmanifestations ofvitamin b …the ocular manifestations of vitamin b-complex deficiency...

Brit. J. Ophihal. (1967) 51, 749

OCULAR MANIFESTATIONS OF VITAMIN B-COMPLEXDEFICIENCY*t

BY

G. VENKATASWAMYDepartment of Ophthalmology, Madurai Medical College, Madurai, South India

VERMA (1942) saw several hundred cases of nutritional amblyopia and blepharo-conjunctivitis in Madras, and reports from the prisoner of war camps in the FarEast showed that blindness can occur as a result of vitamin B-complex deficiency.The use of rice mills instead of the primitive hand-pounding method, by which onlythe husk was removed, and the decreased consumption of millet in urban areas havecaused a high incidence of B-complex deficiency among rice-eating Indians. Thewhite bread produced in India also lacks vitamin B.With few exceptions the resulting ocular lesions cannot be definitely ascribed to a

deficiency of any particular vitamin, and in most cases all the B-complex factors aredeficient.

(1) Angular Conjunctivitis and Blepharo-conjunctivitisLesions of the lid margin similar to those of the lips in riboflavin deficiency are

common. In early cases the lesions appear in the medial and lateral canthi andextend over the whole thickness of the intermarginal strip and some portion of theskin near it. In moderately severe cases where angular stomatitis is associated withcheilosis, the whole length of the lid margins is ulcerated, producing typicalblepharo-conjunctivitis which extends over the intermarginal strip of both eyelids andthe surface of the skin and conjunctiva and even over the naso-labial folds; thelesion may be 0 5 to 1 0 cm. deep with raised and pigmented edges sometimesresembling a rodent ulcer. A case of riboflavin deficiency is shown in Fig. 1.

FiG. I.-Blepharo-conjunctivitis with angular sto-matitis and cheilosis due to ariboflavinosis.

*Received for publication April 12, 1966.t Address for reprints: As above.

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The administration of riboflavin orally and parenterally is followed by totalhealing of these lesions with no residual scar, but they reappear if the patients goback to their old feeding habits.

(2) Corneal VascularizationBessey and Wolbach (1939) drew attention to the occurrence of corneal vasculariza-

tion in riboflavin-deprived rats. Kruse, Sydenstricker, Sebrell, and Cleckley (1940)reported its occurrence in man.

Lyle, Macrae, and Gardiner (1944) examined 4,000 R.A.F. personnel and foundthat corneal vascularity is not necessarily evidence of dietary deficiency. Hills,Liebert, Steinberg, and Horwitt (1951), Youmans, Patton, Robinson, and Kern(1942), Scarborough (1942), Boehrer, Stanford, and Ryan (1943), Williams, Mason,Kusick, and Wilder (1943), and Anderson and Milam (1945) found no correlationbetween corneal vascularization and riboflavin intake.

Tisdall, McCreary, and Pearce (1943), however, found that riboflavin deficiencyalways produced corneal vascularization, and Sebrell (1953) reported a case in whichthe administration of riboflavin caused regression of corneal vascularization and inwhich the capillaries reappeared when the riboflavin was stopped.

Present InvestigationsCases of riboflavin deficiency are frequently seen in the Ophthalmic Department attached

to Madurai Medical College. The incidence of corneal vascularization has been studied inthese patients by means of the slit-lamp microscope.

Method.-Vascularization was graded as follows:(1) Normal limbic plexus with no corneal vessels.(2) Engorgement of limbic plexus with no corneal vessels.(3) Appearance of stray corneal vessels in the cornea with or without engorgement of

limbic plexus.(4) Engorgement of limbic plexus with capillaries extending into the cornea all round the

circumference and forming primary and secondary loops.Material

SERIES 1.-266 patients with signs of ariboflavinosis, such as angular stomatitis andcheilosis, were examined initially. Conditions like trachoma and acute or chronic con-junctivitis and cases of angular stomatitis due to badly-fitting dentures were excluded.Urinary riboflavin estimation and the correction of angular stomatitis and conjunctivitis bythe administration of riboflavin (Venkataswamy, 1960) enabled us to select those with well-established clinical signs of riboflavin deficiency (Table I).

TABLE IRIBOFLAVIN DEFICIENCY WITH CORNEAL VASCULARIZATION IN 266 CASES, BY AGE GROUP

Age Group Corneal Vessels(yrs)

None Few All round Cornea Total

0-10 22 10 1 3311-20 70 29 26 12521-30 33 25 20 7831-40 15 3 4 2241-50 3 2 1 651 and Over 0 1 1 2

Total 143 70 53 266

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OCULAR MANIFESTATIONS OF VITAMIN B-COMPLEX DEFICIENCY 751

SERIES 2.-In the first series of cases the severity of the clinical signs was not noted, anda further study was undertaken of 210 patients in whom the angular stomatitis was gradedas mild, moderate, and severe:

Grade 1.-At the mucous junction of the skin and lips at the angle of the mouth.Grade 2.-Extending on to the skin at the angle of the mouth.Grade 3.-At the angle of the mouth with cheilosis.

The results of slit-lamp observations of the corneal vessels in these patients are given inTable II.

TABLE IIRELATIONSHIP OF SEVERITY OF RIBOFLAVIN DEFICIENCY SYMPTOMS TO CORNEAL

VASCULARIZATION IN 210 CASES

Angular Corneal VesselsStomatitis


Mild 22 21 14 57Moderate 21 29 15 65Severe 29 24 35 88

Total 72 74 64 210

CONTROLS.-447 normal healthy persons, mainly medical students, nurses, and policeconstables, were examined (Table III).

TABLE IIICORNEAL VASCULARIZATION IN 447 NORMAL SUBJECTS, BY AGE GROUP

Age Group Corneal Vessels(yrs)


0-10 1 0 0 111-20 37 42 9 8821-30 53 47 12 11231-40 42 49 14 10541-50 34 42 10 8651 and Over 21 * 32 2 55

Total 188 212 47 447

Results.-In the 447 normal healthy persons, 47 (10 per cent.) had capillaries extendinginto cornea forming loops.

In the 476 patients with riboflavin deficiency (Tables I and 11), there were 117 patientsshowing corneal loops all round and extending into the cornea. The 88 severe cases(Table II) included 35 with extensive corneal loops extending into the cornea. Theincidence ofcorneal vascularization was 39-77 per cent. of the Grade 3 cases. These resultssuggest that corneal vascularization is related to B-complex deficiency, but some severe caseswith marked cheilosis and angular stomatitis showed no corneal vessels, while some mildcases of angular stomatitis and some normal subjects showed extensive cornealvascularization with loop formation. Thus there may be other factors producing cornealvascularization apart from vitamin B2 deficiency.

(3) Epithelial KeratitisAykroyd and Verma (1942) described superficial keratitis with riboflavin deficiency

in India and Metivier (1941) found this condition in Trinidad. It is often seen in the



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FIG. 2.-Moderate riboflavin deficiency with super-ficial comeal ulcer in the right eye.

FIG. 3.--Riboflavin deficiency with epithelialkeratitis in the right eye and corneal ulcerationleading to hypopyon.

Ophthalmic Department, Erskine Hospital, in the form of thin opacities occurring inthe centre of the cornea in the superficial layers (Fig. 2). The patients complain ofdefective vision and photophobia, and corneal opacities of 2 to 3 mm. in diametermay be seen. There is no circumcomeal congestion and there is no association withthe severity of the ariboflavinosis.

In some of these cases the opacity becomes ulcerated and a hypopyon may develop(Fig. 3). In the early stages the lesions heal with vitamin B-complex injections, but

FIG. 4.-Riboflavin deficiency with erosion of medial canthus and epithelialkeratitis.

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in the advanced stage the corneal opacity is permanent. There was no associated lossof corneal sensitivity. This does not appear to be a form of epidemic kerato-conjunctivitis as suggested by McLaren (1963). Numerous case reports and photo-graphs can be produced to support the idea that it is due to vitamin B-complexdeficiency. Keratitis leading to ulceration is shown in Fig. 4.

(4) Nutritional AmblyopiaThe incidence and importance of nutritional amblyopia have not always been

appreciated by ophthalmologists in India, but we found over forty cases in 2 monthsin the Ophthalmic Department of Madurai Medical College. In some the visualacuity was 6/24 or 6/36, but in a few it was as low as 2/60 or even less. This degreeof defect was seen mainly in expectant and nursing mothers; there was no superficialkeratitis or refractive errors and fundus examination showed slight temporal pallorof the optic disc.The vision improved to almost normal when injections of vitamin B-complex were

given. In some cases the improvement was very rapid and a few improved withvitamin B1 and B2 in massive doses. In others, however, only partial improvementwas obtained. It was difficult to estimate the number of people who had poordistance vision or field defect or colour vision defect.

(5) Night BlindnessAccording to Davson (1949) the normal retina contains a very high concentration

of riboflavin, deficiency of which is associated in man with a form of night blindness.We have seen a few cases of ariboflavinosis with a history of night blindness but

some showed no conjunctival changes. They were given injections of only 10 mg.riboflavin a day, and after 10 days there was a marked improvement. Kimble andGordon (1939) stressed the value of riboflavin in improving dark adaptation.Pollak (1945) showed dark-adaptation curves which left little doubt that riboflavinalone can improve dark adaptation, though he did not state whether this was due to adirect action on the retina or to an indirect action through raising the blood level ofvitamin A in the blood. This needs further study.

ConclusionThe ocular lesions of vitamin B-complex deficiency are not as dramatic as those

which occur in keratomalacia, but the number of persons involved is greater. Inmany patients the symptoms of irritation, photophobia, and lacrimation make themunable to do their normal work. The incidence in children of school age was about6 per cent. in our survey. The full impact on working efficiency has not been fullyassessed, but these conditions cause much absenteeism in industry and hamper workin the fields and in the home.

SummaryThe ocular manifestations of vitamin B-complex deficiency include blepharo-

conjunctivitis, epithelial keratitis, nutritional amblyopia, corneal vascularization,night blindness, and general blindness. The first three are definite manifestationsof vitamin B-complex deficiency. Corneal vascularization is seen in a number ofcases, but in this condition other factors may be involved.

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REFERENCESANDERSON, R. K., and MILAM, D. F. (1945). J. Nutr., 30, 17.AYKRoYD, W. R., and VERMA, 0. P. (1942). Indian med. Gaz., 77, 1.BEssEY, 0. A., and WOLBACH, S. B. (1939). J. exp. Med., 69, 1.BICKNELL, F., and PREScoTr, F. (1953). "Vitamins in Medicine", 3rd ed. Heinemann, London.BOEHRER, J. J., STANFORD, C. E., and RYAN, E. (1943). Amer. J. med. Sci., 205, 544.DAVSON, H. (1949). "The Physiology of the Eye", p. 16. Churchill, London.HILLS, O. W., LIEBERT, E., STEINBERG, D. L., and HORWITr, M. K. (1951). Arch. intern. Med., 87, 682.KIMBLE, M. S., and GORDON, E. S. (1939). J. biol. Chem., 128, I ii.KRUSE, H. D., SYDENSTRICKER, V. P., SEBRELL, W. H., and CLECKLEY, H. M. (1940). Publ. Hlth Rep.

(Wash.), 55, 157.LYLE, T. KEITH, MACRAE, T. F., and GARDINER, P. A. (1944). Lancet, 1, 393.MCLAREN, D. S. (1963). "Malnutrition and the Eye", p. 299. Academic Press, New York.MtTIVIER, V. M. (1941). Ibid., 24, 1265.POLLAK, H. (1945). Brit. J. Ophthal., 29, 288.SCARBOROUGH, H. (1942). Brit. med. J., 2, 601.SEBRELL, W. H. Quoted by Bicknell and Prescott (1953), p. 316-317.TISDALL, F. F., MCCREARY, J. F., and PEARCE, H. (1943). Canad. med. Ass. J., 49, 5.VENKATASWAMY, G. (1960). J. All-India ophthal. Soc., 8, 33.VERMA, 0. P. (1942). Indian med. Gaz., 77, 646.WILLIAMS, R. D., MASON, H. L., CUSICK, P. L., and WILDER, R. M. (1943). J. Nutr., 25, 361.YOUMANS, J. B., PATTON, E. W., ROBINSON, W. D., and KERN, R. (1942). Trans. Ass. Amer. Phycns, 57, 49.



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